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Biomedical subjects

M Fujiwara

Publications and source records attributed to M Fujiwara.

At least 883 records · Page 49Linked to original sources
PubMed1978

[Behavioral and EEG effects of triazolam in comparison with those of diazepam (author's transl)].

Triazolam was 4 to 5 times as potent as diazepam in reducing hyperemotionality of either septal-lesioned or olfactory bulbectomized rats (O.B. rats), and in suppressing muricide in O.B. rats. This agent was equipotent with diazepam in inhibiting fighting behavior of long-term isolated mice, but was longer in duration of action. Triazolam was approximately 4 times more potent than diazepam in preventing pentetrazol convulsion, but was 10 times less potent in inhibiting maximal electroshock convulsion in mice. The muscle relaxant effect of triazolam as assessed by the inclined screen test was 34 times, and the effect on rotarod performance was 17 times more potent than that of diazepam in mice. Triazolam (0.2 approximately 0.5 mg/kg i.v.) changed the EEG to a drowsy pattern in unanesthetized rabbits with a chronic electrode implant, and suppressed the EEG arousal response to auditory stimulation and electrical stimulation given to either the mesencephalic reticular formation or posterior hypothalamus. The limbic afterdischarges induced by either hippocampal or amygdaloid stimulation were also markedly inhibited by triazolam. These EEG effects of triazolam were qualitatively similar to, but were 4 to 5 times more potent than those of diazepam. These results indicate that triazolam is a potent tranquilizer with a longer duration of action, and the muscle relaxant effect is considerable as compared with diazepam.

Aggression↗
PubMed1978

Involvement of nicotinic and muscarinic receptors in synaptic transmission in cat superior cervical ganglions reinnervated by vagal primary afferent axons.

Artificial synapses were established in the superior cervical ganglion reinnervated by vagal afferent fibers by heterologous cross-anastomosis between the cranial end of nodose ganglion and the caudal end of superior cervical ganglion in cats. Formation of functional synapses was evidenced by unilateral mydriasis and contraction of the nictitating membrane in response to inflation of the stomach with a balloon or to electrical stimulation of the afferent vagus. Electron microscopic findings indicated that the vagal afferent fibers terminated in the superior cervical ganglion after cross-anastomosis. In the superior cervical ganglion reinnervated by the afferent vagus, activities of choline acetyltransferase and cholinesterase were higher than those in the preganglionically denervated ganglion, but lower than those in the sympathetic preganglionically reinnervated ganglion. Contractions of the nictitating membrane and postganglionic action potentials evoked by electrical stimulation of the vagal artificial preganglionic trunk in the cross-anastomosed ganglion were blocked by treatment with tetraethylammonium and also with atropine. Atropine did not affect these responses in the normal and the preganglionically reinnervated ganglion, except at an early stage after operation. Comparisons of pharmacological properties in normal, anastomosed, preganglionically denervated and reinnervated ganglia indicated that activation of muscarinic receptors in the anastomosed ganglia is probably not secondary to an incomplete nerve supply, but may be dependent on the nature of the nonmyelinated vagal afferent fibers. The possibility that the transmitter involved may be acetylcholine is discussed.

Action Potentials↗
PubMed1978

Antiulcerogenic effect of a pyrido-benzodiazepine derivative (L-S 519) on experimental ulcers.

Effects of a tricyclic, pyrido-benzodiazepnie derivative, 5,11-dihydro-11-[(4-methyl-1-piperazinyl)acetyl]-6H-pyrido[2,3-6][1,4]-benzodiazepin-6-one-dihydrochloride (L-S 519) on experimental ulcers produced by pylorus ligation, cold restraint-stress, and reserpine, and on gastric secretions stimulated by histamine, tetragastrin and carbachol in rats were studied. L-S 519 was half as potent as atropine in preventing these experimental acute ulcers and in decreasing the spontaneous gastric secretion. This compound inhibited to various degrees the gastric secretion stimulated by histamine, tetragastrin and carbachol in acute fistula rats. On the other hand, the antimuscarinic effects of L-S 519 were much weaker than those of atropine in both in vivo and in vitro experiments. Furthermore, the antigastric secretory effect of L-S 519 was observed even in pylorus-ligated, vagotomized rats. By contrast, the effect of L-S 519 was reduced by pretreatment with 6-hydroxydopamine. These results suggest that the adrenergic mechanisms, in addition to a weak antimuscarinic property, are involved in antisecretory and antiulcerogenic effects of L-S 519.

Animals↗
PubMed1977

The effects of destruction of noradrenergic ascending ventral bundles and tetrabenazine on formation of stress-induced gastric ulcer.

The possibility that hypothalamic noradrenaline (NA) plays a role in the formation of gastric ulcers under stress via ventral bundles (VB) was examined in rats after bilateral destruction of VB. After a 3-h restraint stress ulcerative changes were observed in the stomach of sham-operated rats. NA contents in the hypothalamus and cerebral cortex decreased as compared to the respective contents before stress. The VB-lesioning inhibited the stress-induced decrease of NA in the hypothalamus. Ulcer indices in the animals 1 or 7 days after the VB-lesioning, however, did not differ from those of controls. Pretreatment of sham-operated controls with tetrabenazine enhanced the stress-induced decrease of NA in the brain, and exacerbated the gastric ulceration. VB-lesioning completely blocked these effects of tetrabenazine. It appears that the tetrabenazine-induced mobilization of hypothalamic NA via VB causes an aggravation of gastric ulceration.

Adrenergic Fibers↗
PubMed1977

Possible involvement of a central noradrenergic system in automutilation induced by clonidine in mice.

Automutilation induced by a single large dose of clonidine was potentiated by pretreatment with methamphetamine, caffeine and theophyline, while it was inhibited by acute administration of reserpine, alpha-methyl-p-tyrosine, phenoxybenzamine, phentolamine and chlorpromazine. L-Dopa, 5-hydroxytryptophan and p-chlorophenylalanine had no effect on this abnormal behavior. Biochemical studies on brain monoamines revealed that noradrenaline was markedly increased and dopamine slightly so, but 5-hydroxytryptamine was never changed by clonidine. These results suggest that a central noradrenergic system may be involved in automutilation induced by clonidine in mice.

5-Hydroxytryptophan↗
PubMed1977

Effect of PCB (polychlorobiphenyls) on on L-ascorbic acid, pyridoxal phosphate and riboflavin contents in various organs and on hepatic metabolism of L-ascorbic acid in the rat.

Effects of continuous oral administration of PCB (polychlorobiphenyls, 10-100 mg/kg/day, 4 weeks) on tissue levels of L-ascorbic acid (vitamin C), pyridoxal phosphate and riboflavin (vitamin B2) in various organs and on hepatic metabolism of L-ascorbic acid were examined in male Wistar rats weighing 150-250 g. Riboflavin contents in the liver, kidney, brain, heart and testis were not altered by PCB treatments, whereas the hepatic level of pyridoxal phosphate, a biologically active form of vitamin B6, was significantly reduced by PCB administration. Under the same experimental conditions, L-ascorbic acid contents in the liver, kidney, lung and testis showed a significant increase. Histochemical studied revealed that in the adrenal gland, increase of L-ascorbic acid was localized in the fasciculate and reticular zones of cortex, respectively. It was found that increase of L-ascorbic acid in the liver is caused predominantly by activation of biosynthesis at the steps of galactose to D-glucuronic acid and is not due to changes in the catabolic processes of L-ascorbic acid per se. Possible significance of these changes in tissue levels and/or metabolism of vitamins in the occurrence of PCB intoxication is briefly discussed.

Administration, Oral↗